We suggest that the signaling of Aβ42 via α7nAChR contributes prominently to a variety of AD-related neuropathologies in addition to, or perhaps elicited by, tau hyperphosphorylation because these additional neuropathologies are also reduced by PTI-125’s disruption of Aβ42’s signaling via α7nAChR[13,15]. This evidence concerns the gene CHRNA7 and Alzheimer disease.